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This letter to the editor discusses the case of a 58-year-old man with Acute Wernicke Encephalopathy who underwent PET/CT imaging. The imaging revealed increased uptake in the midbrain, medial thalamus, and periaqueductal gray matter, which contrasts with previously reported decreased uptake associated with Wernicke encephalopathy. Treatment with vitamin B1 injection resulted in clinical improvement, and follow-up imaging showed decreased FDG uptake in the cerebral lesion areas. The study suggests that PET/CT can reflect glucose metabolism changes in vital organs affected by thiamine deficiency in Acute Wernicke's encephalopathy. [Extracted from the article]

Purpose: To explore the alterations of whole brain functional network using the degree centrality (DC) analysis in neovascular glaucoma (NVG) and the correlation between DC values and NVG clinical indices. Materials and methods: Twenty NVG patients and twenty normal controls (NC), closely matched in age, sex, and education, were recruited for this study. All subjects underwent comprehensive ophthalmologic examinations and a resting-state functional magnetic resonance imaging (rs-fMRI) scan. The differences in DC values of brain network between NVG and NC groups were analyzed, and correlation analysis was performed to explore the relationships between DC values and clinical ophthalmological indices in NVG group. Results: Compared with NC group, significantly decreased DC values were found in the left superior occipital gyrus and left postcentral gyrus, while significantly increased DC values in the right anterior cingulate gyrus and left medial frontal gyrus in NVG group. (All P < 0.05, FDR corrected). In the NVG group, the DC value in left superior occipital gyrus showed significantly positive correlations with retinal nerve fiber layer (RNFL) thickness (R = 0.484, P = 0.031) and mean deviation of visual field (MDVF) (R = 0.678, P = 0.001). Meanwhile, the DC value in the left medial frontal gyrus demonstrated significantly negative correlations with RNFL (R = − 0.544, P = 0.013) and MDVF (R = − 0.481, P = 0.032). Conclusions: NVG exhibited decreased network degree centrality in visual and sensorimotor brain regions and increased degree centrality in cognitive-emotional processing brain region. Additionally, the DC alterations might be complementary imaging biomarkers to assess disease severity. [ABSTRACT FROM AUTHOR]

Purpose: To explore the alterations of spontaneous neuronal activity and functional connectivity pattern using fractional amplitude of low-frequency fluctuation (fALFF) and functional connectivity (FC) in patients with primary angle-closure glaucoma (PACG) and fALFF relationship with the glaucoma clinical indices. Materials and methods: Forty-two PACG patients and 21 normal controls were enrolled in this study. Resting-state functional magnetic resonance imaging was firstly analyzed by fALFF and brain regions with altered fALFF between groups were selected as seeds for the further FC analysis. The relationships between fALFF/FC values of abnormal regions and ophthalmological measures, including mean deviation of visual field (MDVF) and retinal nerve fiber layer (RNFL) thickness, were also analyzed. Results: Compared with NC, PACG had significant lower fALFF values in the left cuneus, left middle temporal gyrus, right middle temporal gyrus, and right precentral gyrus, while higher fALFF values in the bilateral superior frontal gyrus (P < 0.05 after correction). Furthermore, PACG showed increased FC between left cuneus and bilateral superior frontal gyrus/bilateral posterior cingulate gyrus; between left middle temporal gyrus and bilateral superior frontal gyrus; and between right middle temporal gyrus and bilateral insular (P < 0.05 after correction). In addition, in the PACG group, the mean fALFF values of the left cuneus were positively correlated with MDVF (R = 0.419, P = 0.005) and RNFL thickness (R = 0.322, P = 0.038). Meanwhile, the mean fALFF values of bilateral superior frontal gyrus were negatively correlated with MDVF (R = − 0.454, P = 0.003) and RNFL thickness (R = − 0.556, P < 0.001). Conclusions: PACG exhibited abnormal spontaneous neural activity and connectivity in several brain regions mainly associated with visual and visual-related functions. In addition, the fALFF values of the left cuneus and bilateral superior frontal gyrus may be complementary biomarkers for assessing the disease severity. [ABSTRACT FROM AUTHOR]

This study was performed to understand whether P165 improves learning and memory by restoring insulin action using a diabetes mellitus (DM) rat model. A total of 34 male Sprague-Dawley rats were randomly divided into four groups: control group (n = 8), DM group (n = 8), DM group treated with a low dose of P165 (n = 9), and DM group treated with a high dose of P165 (n = 9). After 8 weeks of treatment, the animals were killed and the expression of insulin signaling-related proteins was examined in the hippocampus by Western blot and immunohistochemical staining. Administration of P165 in diabetic rats did not induce a significant effect on the fasting blood glucose level. The expression of IR, IRS-1, AKT, p-CREB, and Bcl-2 proteins was significantly enhanced in the hippocampus in diabetic rats. Treatment of diabetic rats with P165 at both low and high doses significantly attenuated the expression levels of these proteins. Moreover, immunohistochemistry staining showed that IR, IRS-1, AKT, p-CREB, and Bcl-2 were abundantly expressed in the CA1 region of the hippocampus. The number of cells positively stained for the above proteins was significantly higher in diabetic tissues compared to control tissues, whereas P165 treatments induced a significant reduction in the expression of these proteins. The expression of IR, IRS-1, AKT, p-CREB, and Bcl-2 was enhanced in DM rats, and administration of P165 normalized the expression of these molecules, suggesting that P165 can improve impaired insulin signal transduction. [ABSTRACT FROM AUTHOR]

microRNAs (miRNAs) are a class of small non-coding RNAs, approximately 21-25 nucleotides in length. Recently, some researchers have demonstrated that plasma miRNAs are sensitive and specific biomarkers of various cancers. Using quantitative real-time PCR, the expression levels of miR-454-3p were compared between pre-operative plasmas from 70 glioma patients and 70 healthy controls, and between these pre-operative and post-operative plasmas. Kaplan-Meier analysis was used to evaluate the association of miR-454-3p with prognosis of glioma patients. The expression levels of miR-454-3p in plasma in glioma patients were significantly higher than that from healthy controls. The expression levels of miR-454-3p were higher in high grade gliomas than in low grade gliomas. The AUC of the expression of miR-454-3p in plasma for glioma diagnosis was 0.9063. The expression levels of miR-454-3p in the post-operative plasmas were significantly downregulated when compared to the pre-operative plasmas. Moreover, the prognosis of glioma with high miR-454-3p expression was significantly worse compared with that of glioma with low miR-454-3p expression. Our results suggested that plasma miR-454-3p could be a novel potential diagnostic biomarker for glioma. [ABSTRACT FROM AUTHOR]

We aim to study the therapeutic efficacy of analog P165 of amyloid precursor protein 5-mer peptide in streptozotocin (STZ)-induced cognitive decline model. Rats were divided into four groups: control, STZ, STZ+P165, and STZ+rosiglitazone (RSG). STZ model was established by intracerebroventricular injection of STZ. Three weeks following surgery, rats received daily gavage administration of distilled water (control and STZ groups), P165 (STZ+P165), or RSG (STZ+RSG) for four consecutive weeks. Learning and memory abilities were assessed with the Morris water maze test. Insulin-like growth factor-1 (IGF-1) was detected by ELISA. Expressions of insulin receptor-β (IR-β), insulin receptor substrate-1 (IRS-1), serine/threonine kinase (Akt), and phosphorylation of CREB (p-CREB) were observed by immunohistochemistry. Both P165 and RSG significantly reduced the escape latency relative to the STZ group (P165, P < 0.05; RSG, P < 0.01). STZ model rats had reduced levels of IGF-1 relative to control, and this deficit was attenuated in the STZ+P165 group ( P < 0.01). IR and IRS-1 were elevated in STZ rats, and these levels were restored to near control in the STZ+P165 and STZ+RSG groups ( P < 0.01). Our findings demonstrate that P165 and RSG improved hippocampus-dependent spatial learning and memory in STZ rats by regulating the insulin signaling pathway. [ABSTRACT FROM AUTHOR]

To identify the molecular mechanism underlying improved spatial learning ability of C57/BL mice on a caloric restricted (CR) diet. Seven-week-old male C57/BL mice were randomly divided into three groups: normal control group (NC group, n = 10), high energy group ( n = 10), and low energy group (CR group, n = 10). Body mass and levels of blood glucose were measured every 2 weeks over the course of 30 weeks. After 30 weeks, metabolic parameters, serum total cholesterol, and insulin-like growth factor 1 (IGF-1) were measured, and learning and memory ability of animals were tested using the Morris water maze. The expression of insulin signaling pathway-related proteins in the brain tissues also were tested for molecular mechanism. When compared with the NC group, body weight, and levels of serum glucose decreased in the CR group and increased in the high energy group at all time points tested. Average escape latency and swimming distance were lower in the CR group as compared to the control group after 30 weeks. The serum cholesterol level of the high energy group was significantly higher than that of the control group. The expressions of IGF-1, IR, IRS-1, PI3K, Akt/PKB, and p-CREB protein in the CR group were significantly lower and the expressions of PI3K and Akt/PKB protein in the high energy group were significantly lower than those of the control group at post 30 weeks treatment. Our findings demonstrate that the low energy diet may improve hippocampus-dependent spatial learning ability in C57/BL mice, possibly through a regulatory mechanism of the insulin-PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]